imidacloprid 3

NORTHWEST COALITION FOR ALTERNATIVES TO PESTICIDES/NCAPP. O. B O X 1 3 9 3, E U G E N E, O R E G O N 9 7 4 4 0 / ( 5 4 1 ) 3 4 4 - 5 0 4 4

JOURNAL OF PESTICIDE REFORM/ SPRING 2001 • VOL. 21, NO. 1

15

● I N S E C T I C I D E F A C T S H E E T

Caroline Cox is NCAP’s staff scientist.

BY CAROLINE COX

Imidacloprid (see Figure 1) is a rela-tively new insecticide, first registered foruse as a pesticide in the U.S. in 1994,and was the first insecticide in its chemi-cal class to be developed for commercialuse.1 Imidacloprid is a systemic insecti-cide1; it moves through plants from theplace where it was applied and kills in-sects when they feed. Its major manufac-turer is Bayer Corporation that marketsimidacloprid products with the brandnames Merit, Admire, Premise, Pre-Empt,and Advantage, among others.2-6

Use

Although imidacloprid has not beenin use for long relative to other commonpesticides, according to University of

IMIDACLOPRIDImidacloprid is a relatively new, systemic insecticide chemically related to the tobacco toxin nicotine. Like nicotine,it acts on the nervous system. Worldwide, it is considered to be one of the insecticides used in the largest volume.It has a wide diversity of uses: in agriculture, on turf, on pets, and for household pests.

Symptoms of exposure to imidacloprid include apathy, labored breathing, incoordination, emaciation, andconvulsions. Longer-term exposures cause reduced ability to gain weight and thyroid lesions.

In studies of how imidacloprid affects reproduction, exposure of pregnant laboratory animals resulted in morefrequent miscarriages and smaller offspring.

An agricultural imidacloprid product increased the incidence of a kind of genetic damage called DNA adducts.

Imidacloprid is acutely toxic to some bird species, including sparrows, quail, canaries, and pigeons. Partridges havebeen poisoned and killed by agricultural use of imidacloprid. It has also caused eggshell thinning.

The growth and size of shrimp are affected by imidacloprid concentrations of less than one part per billion (ppb).Shrimp and crustaceans are killed by concentration of less than 60 ppb.

Imidacloprid is persistent. In a field test in Minnesota, the concentration of imidacloprid did not decrease for a yearfollowing treatment. It is also mobile in soil, so is considered by the U.S. Environmental Protection Agency to be apotential water contaminant.

The development of resistance to imidacloprid by pest insects is a significant concern. In Michigan potato fields, theColorado potato beetle developed resistance to imidacloprid after just two years of use.

has a wide variety of uses; it is used inagricultural products for use on cottonand vegetable crops,3 in turfgrass and or-namental plant products,2 in indoor andoutdoor cockroach control products,5 andin termite control products.4 It is alsoused in products for pets, home, lawn,and garden use including some, like pot-ting soil, that may not always be easilyrecognized as pesticides.6,8-10

How Does ImidaclopridKill Insects?

Imidacloprid, and other insecticides inthe nicotinoid chemical family, are “simi-lar to and modeled after the natural nico-tine [a tobacco toxin].”7 (See Figure 2.)Because of their molecular shape, size,and charge, nicotine and nicotinoids fitinto receptor molecules in the nervoussystem that normally receive the moleculeacetylcholine. Acetylcholine carries nerveimpulses from one nerve cell to another,or from a nerve cell to the tissue that a

Arizona entomologist George Ware “verypossibly it is used in the greatest volumeglobally of all insecticides.”7 Imidacloprid

Figure 1Imidacloprid

1-((6-chloro-3-pyridinyl)methyl)-N-nitro-2-imidazolidinimine

Imidacloprid and nicotine have similar activityin the nervous system.

Figure 2Nicotine

N

—CH2

Cl —N-NO2

= NHN

N CH3

N



16

or “other” ingredients. There is little pub-licly available information about the iden-tity of these ingredients. Inerts that havebeen identified in imidacloprid productsinclude the following:

Crystalline quartz silica (in Merit 0.5G13) is classified by the InternationalAgency for Research on Cancer as “car-cinogenic to humans”14 and as “knownto be a human carcinogen”15 by the Na-tional Toxicology Program because itcauses lung cancer. It also causes emphy-sema and obstructive airway disease andhas also caused genetic damage in exposedpeople and laboratory tests.15

Naphthalene (in Leverage 2.716) hasrecently been classified by the NationalToxicology Program as having “clear evi-dence of carcinogenic activity”17 (throughinhalation exposure) because it causes na-sal cancers. It also caused two kinds of

chromosome damage in laboratory tests.17

Other symptoms of naphthalene expo-sure include anemia, liver damage, cata-racts, and skin allergies.18

Whenever possible, the remaining sec-tions of this article will specify whethertests were conducted with imidaclopridalone or with an imidacloprid-contain-ing product (imidacloprid plus inerts).

Toxicity of inerts to cats: An uniden-tified inert ingredient in Advantage, animidacloprid flea insecticide applied asdrops on the back of a pet’s neck, can betoxic to kittens when applied above thelabel rate. In laboratory tests, death, coma,and incoordination were observed in kit-tens receiving five times the recommendeddose of Advantage.19 Further experimentsshowed that the toxicity was probablycaused by the inert present in the largestamount.20 No publicly available studiesshow the effects of smaller overdoses.Vomiting, salivation, and depression werealso observed in cats fed Advantage or itsinert ingredients.21

Acute Toxicity

In laboratory animals, symptoms ofacute (short-term) oral exposure to imida-cloprid included apathy, labored breath-ing, loss of the ability to move, stagger-ing, trembling, and spasms. Some symp-toms lasted for five days following expo-sure.22 Symptoms following acute expo-sure to an agricultural imidacloprid prod-uct (imidacloprid plus “inerts”) includedreduced activity, incoordination, tremors,diarrhea, and emaciation. Some symp-toms lasted 12 days after exposure,23 twiceas long as the symptoms of exposure toimidacloprid alone. (See Figure 3.) Symp-toms following acute exposure to animidacloprid flea control product in-cluded reduced activity, convulsions, andlabored breathing.24

Also in laboratory animals, symptomsof breathing imidacloprid (for four hours)included difficult breathing, loss of theability to move, and slight tremors. Symp-toms of breathing two agricultural imida-cloprid products were similar: incoordi-nation, convulsions, reduced activity,tremors, and salivation. Some symptoms

nerve controls. Imidacloprid and othernicotinoids irreversibly block acetylcho-line receptors.7

Why is imidacloprid less toxic to mam-mals’ nervous systems than to insects’?Both insect and mammal nervous systemshave acetylcholine receptors that areblocked by imidacloprid; most of the sen-sitive receptors are in the central nervoussystem of insects, but in nerves associ-ated with muscles in mammals.7 How-ever, insect acetylcholine receptors aremore sensitive to imidacloprid than aremammalian receptors,11 although forsome of imidacloprid’s breakdown prod-ucts this relationship is reversed.12

Inert Ingredients

Commercial imidacloprid insecticides,like nearly all pesticides, contain ingredi-ents other than imidacloprid called “inert”

In laboratory tests, symptoms of exposure to a commercial imidacloprid product lasted overtwice as long as symptoms of exposure to imidacloprid alone.

Figure 3Persistence of Acute Neurological Symptoms Caused byImidacloprid and a Commercial Imidacloprid Product

Sources:U.S. EPA. Office of Pesticides and Toxic Substances. 1992. Request for experimental usepermit 00315-EUP-ENG and 003125 EUP-ENR for NTN 33893 (Imidacloprid-proposed) acrystalline end-use formulation containing 0.62% NTN 33893 active ingredient. Memo from M.S.Ottley, Health Effects Div., to D. Edwards, Registration Div. Washington, D.C., Mar. 24. (Seeattached Data Evaluation Report for MRID No. 420553-31.)

U.S. EPA. Office of Prevention, Pesticides and Toxic Substances. 1994. Imidacloprid.Evaluation of toxicity data submitted and identification of outstanding toxicology datarequirements. Memo from M.S. Ottley, Health Effects Div., to P. Jenkins and D. Edwards,Registration Div. Washington, D.C., June 8. (See attached Data Evaluation Report for MRID No.428557-02.

Day

s af

ter

expo

sure

12

10

8

6

4

2

0

Imidacloprid Gaucho(imidacloprid + “inert” ingredients)



17

persisted two days after exposure.25

Eye Irritation: Several imidaclopridproducts (Merit 0.5 G,26 Merit 75 WP,2

Premise 75,4 Provado Solupak,27 and Ad-vantage6) cause eye irritation.

Subchronic Toxicity

Subchronic (medium-term; 10-day)exposure of rats to imidacloprid reducedweight gain at a dose of 10 mg/kg perday.28

There are no publicly available sub-chronic studies of commercial imida-cloprid products.

Chronic Toxicity

Chronic (long-term; lifetime) feedingstudies with rats showed that the thyroidis especially sensitive to imidacloprid.Thyroid lesions were caused by doses of17 milligrams per kilogram (mg/kg) ofbody weight per day in males. Slightlyhigher doses (25 mg/kg per day) reducedweight gain in females.29 At higher doses(100 mg/kg per day), effects included at-rophy of the retina in females.30

There are no publicly available chronicstudies of commercial imidaclopridproducts.

Effects on Reproduction

Imidacloprid affects reproduction in avariety of ways. In pregnant rabbits,imidacloprid fed between the sixth andeighteenth days of pregnancy caused anincrease in the frequency of miscarriagesand an increase in the number of off-spring with abnormal skeletons. Theseeffects were observed at a dose of 72 mg/kg per day. In rats, a two generation feed-ing study found that rats fed imidaclopridgave birth to smaller offspring. Theirweight was reduced at a dose of 19 mg/kg per day.31 (See Figure 4.)

There are no publicly available studiesof the effects of commercial imidaclopridproducts on reproduction.

Mutagenicity

The tests of imidacloprid’s ability tocause genetic damage that were submit-ted to the U.S. Environmental ProtectionAgency (EPA) as part of the registration

plants, called the olefine metabolite, ismore toxic to insects than imidaclopriditself.33 Another metabolite, the desnitrometabolite, has very little nervous systemtoxicity to insects33 but is more toxic thanimidacloprid itself in mammals’ nervoussystems.12 The soil metabolite 2-imida-zolidone34 (also known as ethyleneurea)induces tumors in combination with ni-trate35 and causes genetic damage.36

Effects on Birds

Imidacloprid’s acute toxicity to birdsvaries widely among bird species. How-ever, it is “highly toxic”1 to certain spe-cies including house sparrow,1 Japanesequail, canary, and pigeon.37 The medianlethal dose (LD50; dose that kills half of a

process found no evidence of genetic dam-age, or evidence only at high exposures.1

However, a new technique that looks atthe ability of a chemical to cause geneticdamage by chemically binding to DNA(the genetic material) found that theimidacloprid insecticide Admire increasedthe frequency of this kind of damage.DNA adducts (the binding of a chemicalto DNA) were five times more commonin calf thymus cells exposed to Admirethan in unexposed cells.32

Toxicity of Imidacloprid’sMetabolites

Several of imidacloprid’s breakdownproducts (metabolites) can be toxic. Onemetabolite found in imidacloprid-treated

0 4 8 12

Weight of Newborn Offspring

Frequency of miscarriages

Figure 4Effects of Imidacloprid Exposure on Successful Pregnancy

5.0 5.5 6.0

Unexposed

Exposed

Miscarriages (% of total rabbit embryos)

Weight of newborn rats (milligrams)

Unexposed

Exposed

Source:U.S. EPA. Office of Prevention, Pesticides and Toxic Substances. 1993. Imidacloprid.Evaluation of toxicity data submitted and identification of outstanding toxicology datarequirements. Memo from M.S. Ottley, Health Effects Div., to P. Jenkins and D. Edwards,Registration Div. Washington, D.C., Sept. 3. (See attached Data Evaluation Report for MRIDNos. 422563-40 and 422563-39.)

Imidacloprid exposure reduced birth weight 10 percent and doubled the number of miscarriages.



18

test population) for all these species isless than 50 mg/kg.1,37 Based on thesetests, EPA’s Ecological Effects Branchconcluded that the agency’s “levels of con-cern” were exceeded for both non-endangered and endangered songbirds.38

Imidacloprid causes abnormal behav-ior at doses less than 1/5 that which causesdeath. House sparrows fed a granularimidacloprid product showed symptomsof incoordination, lack of responsiveness,and inability to fly at doses of 6 mg/kg.At doses of 12 mg/kg diarrhea and im-mobility were added to the observedsymptoms.39 Even birds for whomimidacloprid is not highly toxic, mallardducks for example, show these symptoms.Symptoms were observed in mallards atall imidacloprid doses used in tests sub-mitted to EPA as part of the registrationprocess.40

Other problems caused by imida-cloprid in birds include eggshell thinning(at exposures of 61 mg/kg),1 decreased

weight (at exposures of 150 ppm infood),41 and reduced egg production andhatching success (at exposures of 234 ppmin food).42

French veterinarians have found deadand poisoned partridges in agriculturalfields following use of imidacloprid-treated seed and verified that the birds’symptoms matched those caused byimidacloprid. Imidacloprid residues werefound in the crop, gizzard, and liver ofthese birds.43

Effects on Fish

Imidacloprid is acutely toxic to adultfish at relatively high concentrations (over80 ppm). Juvenile fish, however are con-siderably more susceptible. Survival ofrainbow trout fry, as well as their weight,was reduced at the lowest imidaclopridconcentration tested (1.2 ppm). There-fore it was not possible to determine thelowest concentration that did not causeadverse effects.44

Effects on OtherAquatic Animals

Imidacloprid is toxic at extremely lowconcentrations to some species of aquaticanimals. The following species have beenstudied as representatives of aquatic ani-mals in general:• The LC50 for the widespread freshwater

crustacean Hyalella azteca is 55 ppb,classified by EPA as very highly toxic.Some mortality was recorded at a con-centration of less than 1 ppb.45

• Imidacloprid’s LC50 for the estuarycrustacean Mysidopsis bahia is 37 ppb.Behavioral effects occurred in those ani-mals that survived exposure: lethargyand loss of equilibrium.46 The LC50for an agricultural imidacloprid prod-uct was similar and EPA also classifiedit as very highly toxic.47 Sublethaleffects on mysid shrimp occurred atstartling low concentrations: length,growth, and production of offspringwere all reduced at concentrations lessthan 1 ppb.48 (See Figure 5.) Mysidshrimp occupy “an important positionin near shore food webs. They consti-tute a major source of food for manyfish species….” In addition, “indirecteffects to waterfowl may be expected ifthe mysid population, or similarorganisms, is depleted.”49

• A study of artificial ponds found thatthe number of invertebrate species andtheir abundance was reduced at con-centrations of 5 ppb.50

Effects on Earthworms

Earthworms are an important part ofthe soil ecosystem. In a typical soil, about80 percent of the animals, by weight, areearthworms. They make important con-tributions to soil fertility and the break-down of organic material.51

Imidacloprid is acutely toxic to earth-worms; for example, the LC50 of the spe-cies Eisenia fetida is between 2 and 4 ppmin soil.51

At lower concentrations, other effectsoccur. The activity of the enzyme cellu-lase, which is found in the earthworm’sgut and allows it to break down plant

Figure 5Effect of Low Concentrations of Imidacloprid on Shrimp

7.5

7.0

6.5

6.0

Shr

imp

leng

th (

mm

) af

ter

28 d

ays

of e

xpos

ure

Unexposed Exposed(.3 ppb)

Length Weight

1.0

.8

.6

.4

.2

0

Shr

imp

wei

ght (

mg)

afte

r 28

day

s of

exp

osur

e

Unexposed Exposed(.3 ppb)

Source:U.S. EPA. Office of Prevention and Toxic Substances. 1992. NTN 33893 ecological effectsdata, response to Miles Inc.’s request to upgrade four aquatic studies. Memo from D. Urban,Ecological Effects Branch, to D. Edwards, Registration Div. Washington, D.C., Aug. 25.

Imidacloprid concentrations of 0.3 ppb reduced growth of mysid shrimp, an important source offood for many saltwater fish species.



19

litter, is reduced by imidacloprid con-centrations of 0.2 ppm.52 The frequencyof deformed sperm in earthworms wasincreased by a soil concentration of 0.2ppm. (See Figure 6.) The frequency ofdamaged DNA (genetic material) inearthworms was increased by a concen-tration of 0.05 ppm.51

Effects on Beneficial Insects

Since imidacloprid is an insecticide, itis not surprising that it is toxic to benefi-cial insects, those that provide an eco-nomic benefit to agriculture. Examplesinclude the following:• Imidacloprid is highly toxic to honey

bees.1

• Lab tests indicated that no adults andonly 10 percent of juvenile spiny sol-dier bugs (a predator of potato beetle,corn earworm, and other pests) wouldsurvive a typical application ofimidacloprid.53

• Treatment of vegetable crops with theimidacloprid insecticide Provado re-duced parasitoids of whiteflies between35 and 50 percent.54

• Treatment of marigolds (with theimidacloprid insecticide Admire) orhoneylocust trees (with theimidacloprid insecticide Merit) in-creased spider mite damage on bothspecies because the insect natural en-emies of the spider mites were killedby the imidacloprid.55 A similar resur-gence of spider mites occurred in egg-plant treated with imidacloprid granulesat planting.56

• Soil treatment of sunflowers, chrysan-themums, and dandelions with imida-cloprid granules (Marathon) caused adecrease in the ability of lady beetles(predators) on the plants to move.57

• An imidacloprid insecticide was acutelytoxic to a variety of predatory insectsin laboratory tests: mirid bugs, lady beetles(adult and larvae), and lacewings.58

Effects on Cats

A British veterinarian reported that acat (that was already ill with cancer) de-veloped a severe skin rash following treat-ment with Advantage. The rash, centered

at the spot where the imidacloprid wasapplied, caused intestinal problems andheart failure, leading to death.59

Effects on Plants

Although it is perhaps surprising foran insecticide, imidacloprid can be toxicto plants. For example, lemon seedlingsgrowing in a greenhouse were damaged bytrunk treatments with an imidacloprid in-secticide,60 and cauliflower seedlings weredamaged by root drench and soil treat-ments.61 In addition, a Polish researcherreported that treatment of peas with theimidacloprid insecticide Gaucho increasedthe incidence of Fusarium root rot.62

Also, an imidacloprid insecticide de-creased growth of blue-green algae anddiatoms at moderate concentrations (9–33 ppm).63,64

Food Contamination

Little monitoring of imidacloprid infood crops is publicly available. The U.S.Department of Agriculture and the Foodand Drug Administration do not include

imidacloprid in their food monitoringprograms.65,66 There are two publishedimidacloprid monitoring studies fromSpain. One found imidacloprid residuesin all samples of greenhouse vegetablestested one week after treatment.67 Theother found imidacloprid in tomatoes,peppers, potatoes, carrots, eggplant, pears,and melons; 21 percent of the sampleswere contaminated.68

Water Contamination

Imidacloprid, according to EPA, “hasthe potential to leach to ground water.In addition, high solubility and mobilityare concerns for transport to surface wa-ter by dissolved runoff.”69 Details aboutthese concerns include the following:• Persistence of imidacloprid varies

among sites in tests submitted as partof its registrations, but is always sig-nificant. The shortest half-life (theamount of time required for half of anapplied pesticide to break down ormove away from the test site) was 107days in turf-covered soil in Georgia.The longest half-life was in Minnesotawhere the imidacloprid concentrationin cornfield soil did not decline for oneyear after treatment.70 (See Figure 7for additional data.)

• Imidacloprid’s ability to move in soil69

has been demonstrated by a variety ofstudies. In a laboratory test, imida-cloprid leached more quickly throughsoil columns than the other 11 pesti-cides tested.71 Some of the other pesti-cides included in this study, diazinon,chlorpyrifos, and diuron, are wide-spread water contaminants.72 EPAmodeled the relative leaching potentialof 14 turf insecticides; imidacloprid wasin category I, pesticides with highestleaching potential.73 When applied ina hop field drip irrigation system,imidacloprid moved to the maximumdepth tested (105 cm) within 7 daysafter application.74 (This represents ahigh-leaching scenario, as the soil wasirrigated daily, but is a good exampleof imidacloprid’s mobility in soil.)Despite the concern raised by these

studies that imidacloprid will contami-

Figure 6Imidacloprid and SpermDeformities in Earthworms

Def

orm

ed s

perm

(%

)

8

6

4

2

0unexposed 0.1 0.2 0.5

(imidacloprid in soil, parts per million)

Source:Luo, Y. 1999. Toxicological study of twonovel pesticides on earthworm, Eiseniafoetida. Chemosphere 39:2347-2356.

Exposure to imidacloprid increases the fre-quency of deformed sperm in earthworms.



20

nate water, EPA did not classify imida-cloprid as a restricted use product in or-der to protect water quality.75 EPA ex-plained their actions this way: “We arenot recommending that the turf and or-namental products be classified as re-stricted use products due to ground wa-ter concerns for several reasons. First, sev-eral of the proposed NTN products con-tain directions for use around the homeand a Restricted Use Classification wouldnot allow sale of these products to thehomeowner. Second, professional lawncare companies will be users of these prod-ucts and they will not use a RestrictedUse Product.”76 Thus, the decision wasan economic one, not a scientific one.

Resistance

The development of resistance toimidacloprid in pest species appears tobe a serious concern. In Michigan,

imidacloprid resistance in the Coloradopotato beetle was documented followingtwo years of imidacloprid use on pota-toes. (In both years, over 80 percent ofthe potato acreage was treated withimidacloprid.)77 In laboratory experi-ments, thrips selected for their resistanceto the organophosphate insecticidediazinon were also resistant to imida-cloprid.78 This situation, in which resis-tance to one insecticide confers resistanceto another insecticide, is called cross-re-sistance and is “especially disconcerting”78

to the University of Missouri researcherswho conducted the study.

References1. U.S. EPA. Office of Pesticide Programs. 1994.

Pesticide fact sheet: Imidacloprid. Washington,D.C., Mar. 18.

2. Bayer Corporation. 2000. Merit® 75 WP. Speci-men label. Kansas City MO, May 18. http://pro-tect-your-turf.com.

3. Bayer Corporation. 1999. Admire® 2 Flowable.

Specimen label. Kansas City MO, Aug. 3. http://uscrop.bayer.com.

4. Bayer Corporation. 1999. Premise® 75. Speci-men label. Kansas City MO, Jan. 4. http://usagri.bayer.com.

5. Bayer Corp. 1999. Pre-EmptTM. Specimen la-bel. Kansas City MO, Apr. 19. http://usagri.bayer.com.

6. Bayer Corp. 1999. Advantage®. Specimen la-bel. Shawnee Mission, Kansas 66201 MO, Jan.4. http://www.nofleas.com.

7. Ware, G.W. The pesticide book. Fresno CA:Thomson Publications. Pp. 68, 180-184.

8. Bayer-Pursell, LLC. Undated. Bayer Advanced Gar-den product guide. www.BayerAdvanced.com.

9. California Dept. of Pesticide Regulation. 2000.Database entry for Bayer Advanced Garden 2-in-1 Plant Spikes Fertilizer + Insecticide 8-11-5Ready-to-Use, Feb. 13. www.cdpr.ca.gov/docs/label/prodnam.htm.

10. California Dept. of Pesticide Regulation. 2000.Database entry for Bayer Advanced Lawn Sea-son-Long Grub Control Ready-to-Use, Feb. 13.www.cdpr.ca.gov/docs/label/prodnam.htm.

11. Zwart, R., M. Oortgiessen, and H.P.M. Vijver-berg. 1994. Nitromethylene heterocycles: Se-lective agonists of nicotinic receptors in locustneurons compared to mouse N1E-115 andBC3H1 cells. Pestic. Biochem. Physiol. 48:202-213.

12. Tomizawa, M. and J.E. Casida. 1999. Minorstructural changes in nicotinoid insecticides con-fer differential subtype selectivity for mamma-lian nicotinic acetylcholine receptors. Brit. J.Pharmacol. 127:115-122.

13. Bayer Corp. 1994. Material safety data sheet:Merit 0.5 G Insecticide. Kansas City, MO, Sept.23.

14. International Agency for Research on Cancer.1997. Silica. http://193.51.164.11/htdocs/Mono-graphs/Vol68/SILICA.HTM.

15. U.S. Dept. of Health and Human Services. Pub-lic Health Service. National Toxicology Program.2000. Ninth Report on Carcinogens. http://ehis.niehs.nih.gov/roc/toc9.html.

16. Bayer Corp. 1994. Material safety data sheet:Leverage. Kansas City, MO, Sept.

17. National Toxicology Program. Undated. Toxicol-ogy and carcinogenesis studies of naphthalene(CAS No. 91-20-3) in F344/N rats (inhalationstudies). TR-500. http://ntp-server.niehs.nih.gov/htdocs/LT-studies/TR500.html.

18. Acros Organics. 1999. Material safety data sheet:Naphthalene, 99%. Fair Lawn, NJ.www.fishersci.com.

19. Bayer Corp. Agricultural Div. 1996. Letter fromT. McNamara, biochemistry and pesticides reg-istration manager, to U.S. EPA Office of Pesti-cide Programs, 6(a)(2) document processingdesk, June 17.

20. Bayer Corp. Agricultural Div. 1996. Generalsafety evaluation for topical use of imidacloprid(AdvantageTM) Spot-On on six week old kittens.Shawnee Mission, KS, Aug. 20.

21. Bayer Corp. Agricultural Div. 1996. Acute oraltoxicity evaluation of imidacloprid (AdvantageTM)in cats. Shawnee Mission, KS, Nov. 11.

22. U.S. EPA. Office of Pesticides and Toxic Sub-stances. 1992. Request for experimental use per-mit 00315-EUP-ENG and 003125 EUP-ENR forNTN 33893 (Imidacloprid-proposed) a crystal-line end-use formulation containing 0.62% NTN33893 active ingredient. Memo from M.S. Ottley,Health Effects Div., to D. Edwards, RegistrationDiv. Washington, D.C., Mar. 24. (See attachedData Evaluation Report for MRID No. 420553-31.)

23. U.S. EPA. Office of Prevention, Pesticides andToxic Substances. 1994. Imidacloprid. Evalua-

FIgure 7Persistence of Imidacloprid in Soil in Three States

3mos.

> 1year

> 1year

4mos.

Note:Length of bar is proportional to the soil half-life, in days. Half-life is the length of timerequired for half of the applied imidaclopridto break down or move away from theapplication site.

Source:U.S. EPA. Environmental Fate and Groundwater Branch. 1993. EFGWB review ofimidacloprid. Washington, D.C., Jun 11. Pp. 5-6 and attached pesticide environmental fate oneline summary.

Imidacloprid is persistent in soil. In some studies, over half of the applied imidacloprid is stillpresent one year after application.

turf

bare soil

corn

tomatoes



21

tion of toxicity data submitted and identificationof outstanding toxicology data requirements.Memo from M.S. Ottley, Health Effects Div., toP. Jenkins and D. Edwards, Registration Div.Washington, D.C., June 8. (See attached DataEvaluation Report for MRID No. 428557-02.)

24. U.S. EPA. Office of Prevention, Pesticides andToxic Substances. 1996. Imidacloprid. Evalua-tion of product labeling data submitted and iden-tification of outstanding toxicology data require-ments. Memo from M.S. Ottley, Health EffectsDiv., to P. Jenkins and D. Edwards, Registra-tion Div. Washington, D.C., Mar. 5. p. 6.

25. Ref. # 23. (See p. 5 and attached Data Evalua-tion Report for MRID No. 428557-04.)

26. Bayer Corp. 1998. Merit® 0.5 G. Specimen la-bel. Kansas City MO, Sept. 30. http://protect-your-turf.com.

27. Bayer Corp. Undated. Provado® Solupak. Speci-men label. Kansas City MO. http://uscrop.bayer.com.

28. U.S. EPA. Office of Prevention, Pesticides andToxic Substances. 1993. Imidacloprid. Evalua-tion of toxicity data submitted and identificationof outstanding toxicology data requirements.Memo from M.S. Ottley, Health Effects Div., toP. Jenkins and D. Edwards, Registration Div.Washington, D.C., Sept. 3. p. 8.

29. U.S. EPA. Office of Pesticides. 1994. Toxoneliners: Imidacloprid. Washington, D.C., Jan.3. p.1.

30. U.S. EPA. Office of Prevention, Pesticides andToxic Substances. 1993. Imidacloprid. Evalua-tion of toxicity data submitted and identificationof outstanding toxicology data requirements.Memo from M.S. Ottley, Health Effects Div., toP. Jenkins and D. Edwards, Registration Div.Washington, D.C., Jan. 11. (See attached DataEvaluation Report for MRID Nos. 422563-31 and422563-32.)

31. Ref. # 28. See attached Data Evaluation Reportfor MRID Nos. 422563-40 and 422563-39.

32. Shah, R.G. et al. 1997. Determination ofgenotoxicity of the metabolites of the pesticidesGuthion, Sencor, Lorox, Reglone, Daconil, andAdmire by 32P-postlabeling. Mol. Cell. Biochem.169:177-184.

33. Nauen, R. et al. Efficacy of plant metabolites ofimidacloprid against Myzus persicae and Aphisgossypii (Homoptera: Aphididae). Pestic. Sci.52:53-57.

34. Rouchaud, J., F. Gustin, and A. Wauters. 1996.Imidacloprid insecticide soil metabolism in sugarbeet field crops. Bull. Environ. Contam. Toxicol.56:29-36.

35. Sander, J. and Buerkle, G. 1971. Induction ofmalignant tumors in rats by oral administrationof 2-imidazolidinone and nitrite. Z. Krebsforsch75(4):301-304. (Abstract.)

36. Szegedi, M. 1983. Comparative mutagenic in-vestigation of the decomposition products ofalkylene bis(dithiocarbamate) fungicides andNeviram 80WP. Nehezvegyip. Kut. Intez. Kozl.14:37-51. (Abstract.)

37. U.S. EPA. Office of Prevention, Pesticides andToxic Substances. 1994? Imidacloprid, avian6(a)(2) submittals. Memo from A.F. Maciorowski,Ecological Effects Branch, to D. Edwards, Reg-istration Div. Washington, D.C.

38. U.S. EPA. 1993. Ecological effects preliminaryreview. NTN 33893-2 systemic insecticide.Washington, D.C., Feb. 5.

39. U.S. EPA. 1992. Data evaluation record: NTN33893. MRID No. 420553-09. Washington, D.C.,Mar. 27.

40. Bayer Corp. Agriculture Div. 1996. NTN 33893technical: An acute oral LD50 with mallards.440594-01. Stilwell, KS, June 20.

41. U.S. EPA. 1992. Data evaluation record: NTN

33893. MRID No. 420553-11. Washington, D.C.,Mar. 27.

42. U.S. EPA. 1992. Data evaluation record: NTN33893. MRID No. 420553-13. Washington, D.C.,Aug. 24.

43. Berny, P.J. et al. 1999. Evaluation of the toxicityof imidacloprid in wild birds. A new high perfor-mance thin layer chromatography method for theanalysis of liver and crop samples in suspectedpoisoning cases. J. Liq. Chrom. & Rel. Technol.22:1547-1559.

44. U.S. EPA. 1992. Addendum: Data evaluationrecord. MRID Nos. 420553-20 and 424805-01.Washington, D.C.

45. U.S. EPA. Office of Prevention, Pesticides andToxic Substances. 1992. NTN 33893 (imida-cloprid), data evaluation records. Memo fromA.F. Maciorowski, Ecological Effects Branch, toD. Edwards, Registration Div. Washington, D.C.,Dec. 22. (See attached Data Evaluation Reportfor MRID Nos. 422563-03.)

46. U.S. EPA. 1992. Data evaluation record: NTN33893. MRID No. 420553-19. Washington, D.C.,Mar. 27.

47. U.S. EPA. Office of Prevention and Toxic Sub-stances. 1993. NTN 33893 240 FS formulationacute Mysid study. Memo from A.F. Maciorowski,Ecological Effects Branch, to D. Edwards, Reg-istration Div. Washington, D.C., Feb. 9. (Seeattached Data Evaluation Report for MRID No.425283-01.)

48. U.S. EPA. Office of Prevention and Toxic Sub-stances. 1992. NTN 33893 ecological effectsdata, response to Miles Inc.’s request to up-grade four aquatic studies. Memo from D. Ur-ban, Ecological Effects Branch, to D. Edwards,Registration Div. Washington, D.C., Aug. 25.

49. U.S. EPA. Office of Prevention and Toxic Sub-stances. 1993. Reconsideration of non-food userisk assessments for NTN 33893 [2.5% granu-lar, 0.62% granular, NTN 33893-2 flowable].Memo from A.F. Maciorowski, Ecological EffectsBranch, to D. Edwards, Registration Div. Wash-ington, D.C., May 6.

50. U.S. EPA. Office of Prevention and Toxic Sub-stances. 1993. Screen of the NTN 33893 micro-cosm study. Memo from A.F. Maciorowski, Eco-logical Effects Branch, to D. Edwards, Registra-tion Div. Washington, D.C., Apr. 19. p. 10.

51. Zang, Y. et al. 2000. Genotoxicity of two novelpesticides for the earthworm, Eisenia fetida.Environ. Pollut. 108:271-278.

52. Luo, Y. 1999. Toxicological study of two novelpesticides on earthworm, Eisenia foetida.Chemosphere 39:2347-2356.

53. De Cock, A. et al. 1996. Toxicity of diafenthiuronand imidacloprid to the predatory bug Podisusmaculiventris (Heteroptera: Pentatomidae).Environ. Entomol. 25:476-480.

54. Simmons, A.M. and D.M. Jackson. 2000. Evalu-ation of foliar-applied insecticides on abundanceof parasitoids of Bemesia argentifolii (Homoptera:Aleyrodidae) in vegetables. J. Entomol. Sci. 35:1-8.

55. Sclar, D.C., D. Gerace. and W.S. Cranshaw.1998. Observations of population increases andinjury by spider mites (Acari: Tetranychidae) onornamental plants treated with imidacloprid. J.Econ. Entomol. 91:250-255.

56. Nemoto, H. 1995. Pest management systemsfor eggplant arthropods: A plan to control pestresurgence resulting from the destruction of natu-ral enemies. JARQ 29:25-29.

57. Smith, S.F. and V.A. Krischik. 1999. Effects ofsystemic imidacloprid on Coleomegilla maculata(Coleoptera: Coccinellidae). Environ. Entomol.28: 1189-1195.

58. Mizell, R.F. and M.C. Sconyers. 1992. Toxicityof imidacloprid to selected arthropod predators

in the laboratory. Flor. Entomol. 75:277-280.59. Godfrey, D.R. 1999. Dermatosis and associated

systemic signs in a cat with thymoma and re-cently treated with an imidacloprid preparation.J. Small Anim. Pract. 40:333-337.

60. Bullock, R.C. and R.R. Pelosi. 1993. Toxicity ofimidacloprid to selected arthropods in the citrusgreenhouse and grove. Proc. Fla. State Hort.Soc. 106: 42-47.

61. Natwick, E.T., J.C. Palumbo, and C.E. Engle.1996. Effects of imidacloprid on colonization ofaphids and silverleaf whitefly and growth, yieldand phytotoxicity in cauliflower. Southwest.Entomol. 21:283-292.

62. Burgiel, Z.J. 1998. Effects of some pesticideson the healthiness of pea. Chem. Inz. Ekol.5:553-562. (Abstract.)

63. Bayer Corp. Agriculture Division. 1996. Toxicityof NTN 33893 2F to the blue-green algae Ana-baena flos-aquae. Kansas City MO, Dec. 3.

64. Bayer Corporation. Agriculture Division. 1996.Toxicity of NTN 33893 2F to the freshwater dia-tom Navicula pelliculosa. Kansas City MO, Dec.2.

65. U.S. Dept. of Agriculture. Agricultural MarketingService. Science and Technology. 2001. Pesti-cide data program: Annual summary calendaryear 1999. Appendix E.

66. U.S. Food and Drug Admin. Undated. Food andDrug Administration Pesticide Program: Residuemonitoring 1999. Washington, D.C. http://vm.cfsan.fda.gov/~dms/pesrpts.html. Table 3.

67. Fernandez-Alba, A.R. et al. 1996. Determina-tion of imidacloprid in vegetables by high-per-formance liquid chromatography with diode-ar-ray detection. J. Chromatogr. A 721:97-105.

68. Fernandez-Alba, A.R. et al. 2000. Determina-tion of imidacloprid and benzimidizole residuesin fruits and vegetables by liquid chromatogra-phy-mass spectrometry after ethyl acetate multi-residue extraction. J. AOAC Intern. 83:748-755.

69. U.S. EPA. Environmental Fate and Groundwa-ter Branch. 1993. EFGWB review of imidacloprid.Washington, D.C., Jun 11. p. 3.

70. Ref. #69, pp. 5-6 and attached pesticide envi-ronmental fate one line summary.

71. Vollner, L. and D. Klotz. 1997. Leaching anddegradation of pesticides in groundwater layers.In Environmental behaviour of crop protectionchemicals. Vienna, Austria: International AtomicEnergy Agency. Pp. 187-203.

72. U.S. Geological Survey. 1999. The quality ofour nation’s waters—nutrients and pesticides.Circular 1225. Reston VA: USGS. p. 60.

73. U.S. EPA. 1993. Comparison of the leachingpotential of imidacloprid (NTN) to other turf in-secticides considered in the preliminary turfcluster assessment. Memo from J. Wolf, soil sci-entist, to H. Jacoby, chief. Washington, D.C.,June 15.

74. Felsot, A.S., et al. 1998. Distribution of imida-cloprid in soil fol lowing subsurface dripchemigation. Bull. Environ. Contam. Toxicol.60:363-370.

75. U.S. EPA. 2000. Office of Pesticide Programs.Restricted use products (RUP) report. Washing-ton, D.C., Oct. www.epa.gov/RestProd/rupoct00.htm.

76. U.S. EPA. 1994. Registration for imidacloprid(NTN 33893). Memo from S.J. Johnson, Regis-tration Div., to D.D. Campt, Office of PesticidePrograms. Washington, D.C., Mar. 10.

77. Grafius, E.J. and B.A. Bishop. 1996. Resistanceto imidacloprid in Colorado potato beetles fromMichigan. Res. Pest Manage. 8:21-26.

78. Zhao, G. et al. 1995. Insecticide resistance infield and laboratory strains of western flowerthrips (Thysanoptera: Thripidae). J. Econ.Entomol. 88:1164-1170.

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